SIRT3 inactivation promotes acute kidney injury through elevated acetylation of SOD2 and p53

The elevation of SOD2 and p53 protein acetylation in the mitochondria of renal tubular epithelial cells is an important signaling event in the pathogenesis of I/R-induced AKI. Thus, deacetylase SIRT3 may be an upstream regulator of both SOD2 and p53, and the SIRT3 deactivation may aggravate AKI.